In:
Journal of Biomaterials and Tissue Engineering, American Scientific Publishers, Vol. 11, No. 6 ( 2021-06-01), p. 1129-1137
Abstract:
The epithelial-mesenchymal transition (EMT) of bronchial epithelial cells is a critical mechanism involved in transforming growth factor beta 1 (TGF- β 1) induced asthma airway remodeling. Previous study has shown that interleukin 27 (IL-27) attenuates EMT in alveolar epithelial
cells, but its effects on the BEAS-2B human bronchial epithelial cell line EMT remain unknown. Herein, we explored the effects of IL-27 on BEAS-2B EMT in vivo and in vitro . In the in vivo experiments, we found that IL-27 nose-drip therapy alleviated airway remodeling, increased
the epithelial phenotypic marker epithelial-cadherin (E-cadherin), and decreased the mesenchymal phenotypic marker alpha-smooth muscle actin ( α -SMA) compared with the asthmatic control group. We also found that IL-27 suppressed the signal transducer and activator of transcription
(STAT3) in the lung tissue of asthmatic mice. in vitro , TGF- β 1-induced EMT changes, including downregulation of E-cadherin and upregulation of α -SMA, were suppressed by IL-27 treatment. Additionally, STAT3 phosphorylation was activated by TGF- β 1,
whereas IL-27 inhibited the activation of TGF- β 1 induced STAT3 phosphorylation. Our findings indicated that IL-27 could inhibit airway remodeling by attenuating bronchial epithelial cell EMT in vivo and in vitro . Therefore, IL-27 may be a beneficial therapeutic option
targeting asthmatic airway remodeling.
Type of Medium:
Online Resource
ISSN:
2157-9083
DOI:
10.1166/jbt.2021.2669
Language:
English
Publisher:
American Scientific Publishers
Publication Date:
2021
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